This study aims to determine whether dysfunctional High Density Lipoprotein (HDL) influenced the expression of scavenger receptor class B type Ⅰ (SR-B1) to determine reverse cholesterol transport. Blood samples obtained from coronary heart disease patients confirmed by angiography were collected. HDL was extracted from the blood via ultracentrifugation. Then, the HDL was injected into apoE-/- mice, and the HepG2 cells cultured with Dulbecco's modified eagle medium (DMEM) were added the HDL extracted from coronary heart disease patients. As controls, normal cases without coronary heart disease (CHD) and patients with angina pectoris and acute myocardial infarction were used. The protein expression levels of SR-B1 were detected by western blot, and the lipid accumulation levels were detected by Oil Red O staining in both tissues and cell levels. These results revealed that the HDL obtained from CHD patients downregulate the SR-B1 expression in ex vitro and in vitro studies. In addition, dysfunctional HDL may result in lower SR-B1 expression levels. The degree of SR-B1 expression levels could be relative to the degree of coronary congestion. Along with the increase in severe coronary congestion, such as myocardial infarction, the SR-B1 expression levels were lower. The dysfunctional HDL derived from coronary heart disease patients decreased the expression of SR-B1, and promoted lipid accumulation.
Keywords: atherosclerosis; coronary heart disease; dysfunctional HDL; reverse cholesterol transport; scavenger receptor BI.